Key result
Electrical field stimulation and methoxamine cause the release of ATP from rat caudal artery, suggesting both neuronal and extraneuronal sites contribute to ATP overflow.
Both neuronal and extraneuronal sites may contribute to the overflow of ATP in the rat caudal artery following stimulation.
Does not inform clinical vascular management; leaves open extraneuronal ATP contributions in human arteries.
Electrical field stimulation of the rat caudal artery (0.5-ms pulses at 8 Hz for 3 min) results in the release of norepinephrine (quantified by HPLC-electrochemical detection) and adenyl purines including ATP, ADP and AMP (quantified by HPLC-fluorescence detection). The amount of ATP released from the tissue exceeded the amount of norepinephrine. Because postjunctional alpha 1-adrenoceptor stimulation with methoxamine also causes release of ATP, both neuronal and extraneuronal sites may contribute to the overflow of ATP. Results with the alpha 1-adrenoceptor antagonist prazosin lend support to this notion. Prazosin (10(-6) M) completely blocked the release of ATP by methoxamine but only partially reduced the release of ATP by field stimulation.
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Westfall et al. (2008) studied this question. Electrical field stimulation was evaluated on Release of norepinephrine and adenyl purines (ATP, ADP, AMP). Electrical field stimulation and methoxamine cause the release of ATP from rat caudal artery, suggesting both neuronal and extraneuronal sites contribute to ATP overflow.
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